Brain Volume Regulation in Response to Hypo-osmolality and Its Correction
Section snippets
Brain volume regulation and the consequences of hyponatremia
The osmolality of extracellular and intracellular fluid must be equal. If extracellular osmolality is reduced, cells must either swell with water or rid themselves of solute. Because water is able to cross the blood-brain barrier much more readily than sodium, a low serum sodium concentration osmotically drives water flow into the brain’s interstitial space and into brain cells. However, the severity of the induced brain swelling diminishes with time.
Initially, the increase in brain water
Brain composition in acute versus chronic hyponatremia
In animals that have hyponatremia for <24 hours, cerebral edema is severe and rapid correction of hyponatremia returns brain water content to normal with no adverse consequences.8 After 3 days of hyponatremia, brain swelling is minimal and brain histology remains normal, even when the serum sodium concentration is maintained at very low levels for several weeks.14 However, if more sustained hyponatremia is rapidly corrected, the animals deteriorate neurologically and myelinolysis develops.8, 15
Urea and myelinolysis
Intravenous and oral urea are commonly used in Belgium to treat hyponatremia.26 Van Reeth and Decaux27 noted that rapid correction of hyponatremia with urea in an animal model of severe hyponatremia did not appear to cause myelinolysis. Nephrologists know that a rapid increase of the serum sodium concentration is extremely common in patients receiving dialysis, yet myelinolysis in this population is also very rare. Exploring these observations, Soupart and coworkers20, 28 demonstrated that
Myoinositol and myelinolysis
If urea protects against injury and this protection is associated with a rapid uptake of brain myoinositol in the brain, can myoinositol be given exogenously to protect against brain injury due to rapid correction of chronic hyponatremia? Studies in our laboratory have shown that hyponatremic animals have brain myoinositol levels that are approximately 50% of those of normonatremic controls. If myoinositol is administered in conjunction with hypertonic saline to hyponatremic animals (increasing
Clinical guidelines
Our knowledge of the brain’s adaptation to hyponatremia can be applied to the bedside. All patients with a serum sodium concentration <120 mEq/L (i.e., >10% below normal) have adapted to some degree because the brain cannot increase its volume by >10% without herniating. The recovery of brain solutes during correction of hyponatremia is slower than is the loss of brain solutes during the evolution of hyponatremia. Therefore, correction rates should not exceed a 10% increase in sodium
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2022, American Journal of Emergency MedicineAssociation of optic nerve sheath diameter measurement with hyponatremia in emergency department
2019, American Journal of Emergency MedicineCitation Excerpt :No significant difference was noted between the admission and discharge ONSDs of the admitted patients and patients discharged from the emergency department (p > 0.05). Although several studies reported that hyponatremia causes ICP elevation, no study to date has investigated the relationship between hyponatremia-induced intracranial pressure increase and ONSD [4-8]. Nevertheless, it is already known that ONSD reflects ICP in many pathological conditions (intracranial bleeding, stroke, pseudotumor cerebri) [9-16].
Practical document on the management of hyponatremia in critically ill patients
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